DESCRIPTION: (Adapted from Abstract) A class of zebra fish motility mutants that are motile and can swim but do not respond to touch have been isolated. One of these mutants is termed mao. The phenotype of these mutants suggests that the defect may originate in mechanosensory Rohon-Beard (RB) neurons. Normally, the action potential of RB cells undergoes developmental regulation so that the embryo acquires touch sensitivity. The embryos of mao zebra fish do not acquire such sensitivity. The changes in action potential waveform in RB cells are due to underlying changes in voltage-gated sodium and potassium currents. The RB cells of mao zebra fish have reduced sodium current amplitudes, and action potentials are not generated. In addition, up regulation of sodium current is not observed, even though the normal developmental changes in potassium currents do occur. These data suggest that developmental regulation of RB sodium current may underlie stage-specific acquisition of touch sensitivity. To investigate this possibility, the investigator will examine three specific aims. The first aim is to dissect RB whole-cell sodium current into underlying pharmacological and functional components. The second aim is to identify the classes of voltage-dependent sodium channel genes expressed in RB cells. The final aim is to compare the morphological properties of RB cells in wildtype and mao mutant embryos.